Sun Chenglong, Guo Yunxue, Tang Kaihao, Wen Zhongling, Li Baiyuan, Zeng Zhenshun, Wang Xiaoxue
Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Key Laboratory of Marine Materia Medica, RNAM Center for Marine Microbiology, South China Sea Institute of Oceanology, Chinese Academy of SciencesGuangzhou, China.
University of Chinese Academy of SciencesBeijing, China.
Front Microbiol. 2017 May 9;8:840. doi: 10.3389/fmicb.2017.00840. eCollection 2017.
Bacterial toxin/antitoxin (TA) systems have received increasing attention due to their prevalence, diverse structures, and important physiological functions. In this study, we identified and characterized a type II TA system in a soil bacterium KT2440. This TA system belongs to the MqsR/MqsA family. We found that PP_4205 (MqsR) greatly inhibits cell growth in KT2440 and , the antitoxin PP_4204 (MqsA) neutralizes the toxicity of the toxin MqsR, and the two genes encoding them are co-transcribed. MqsR and MqsA interact with each other directly and MqsA is a negative regulator of the TA operon through binding to the promoter. Consistent with the MqsR/MqsA pair in , the binding of the toxin MqsR to MqsA inhibits the DNA binding ability of MqsA in KT2440. Disruption of the gene which induces expression increases persister cell formation 53-fold, while overexpressing which represses expression reduces persister cell formation 220-fold, suggesting an important role of MqsR in persistence in KT2440. Furthermore, both MqsR and MqsA promote biofilm formation. As a DNA binding protein, MqsA can also negatively regulate an ECF sigma factor AlgU and a universal stress protein PP_3288. Thus, we revealed an important regulatory role of MqsR/MqsA in persistence and biofilm formation in KT2440.
细菌毒素/抗毒素（TA）系统因其广泛存在、结构多样和重要的生理功能而受到越来越多的关注。在本研究中，我们在土壤细菌KT2440中鉴定并表征了一个II型TA系统。该TA系统属于MqsR/MqsA家族。我们发现PP_4205（MqsR）在KT2440中极大地抑制细胞生长，抗毒素PP_4204（MqsA）中和毒素MqsR的毒性，并且编码它们的两个基因共转录。MqsR和MqsA直接相互作用，并且MqsA通过与启动子结合成为TA操纵子的负调节因子。与KT2440中的MqsR/MqsA对一致，毒素MqsR与MqsA的结合抑制了KT2440中MqsA的DNA结合能力。诱导mqsR表达的基因的破坏使持留细胞形成增加53倍，而过度表达抑制mqsR表达的基因使持留细胞形成减少220倍，这表明MqsR在KT2440的持留中起重要作用。此外，MqsR和MqsA都促进生物膜形成。作为一种DNA结合蛋白，MqsA还可以负调节一个ECF西格玛因子AlgU和一个普遍应激蛋白PP_3288。因此，我们揭示了MqsR/MqsA在KT2440的持留和生物膜形成中的重要调节作用。
